期刊
NATURE GENETICS
卷 45, 期 1, 页码 98-U143出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.2481
关键词
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资金
- Japan Society for the Promotion of Science (JSPS) KAKENHI [10J02434, 21229009, 23590937, 24229005, 24659363, 24590914, 24590916]
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Ministry of Health, Labour and Welfare, Japan
- Ministry of Education, Culture, Science, Sports and Technology of Japan [LS075]
- Princess Takamatsu Cancer Research Fund [10-24212]
- Grants-in-Aid for Scientific Research [23590937, 13J02261] Funding Source: KAKEN
There is great interest in tumor stem cells (TSCs) as potential therapeutic targets; however, cancer therapies targeting TSCs are limited. A drawback is that TSC markers are often shared by normal stem cells (NSCs)(1-4); thus, therapies that target these markers may cause severe injury to normal tissues. To identify a potential TSC-specific marker, we focused on doublecortin-like kinase 1 (Dclk1). Dclk1 was reported as a candidate NSC marker in the gut(5,6), but recent reports have implicated it as a marker of differentiated cells (for example, Tuft cells)(7,8). Using lineage-tracing experiments, we show here that Dclk1 does not mark NSCs in the intestine but instead marks TSCs that continuously produce tumor progeny in the polyps of Apc(Min/+) mice. Specific ablation of Dclk1-positive TSCs resulted in a marked regression of polyps without apparent damage to the normal intestine. Our data suggest the potential for developing a therapy for colorectal cancer based on targeting Dclk1-positive TSCs.
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